Interestingly, in the presence of HOE 642, the calculated reversal potential of the glutamate transported at 5 h REOX was −57.94 mV (vs. −78.2 mV at OGD/REOX), suggesting that inhibition of NHE1 and subsequent reduction of Na+ overload would help to prevent EEATs-mediated glutamate release from astrocytes following ischemia. Here, SLC9A1 is linked to ischemia.